Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder characterized by reduced circulating levels and/or impaired function of alpha-1 antitrypsin (AAT), a key serine protease inhibitor, in which loss of effective antiprotease protection results in unchecked neutrophil elastase activity and progressive lung tissue destruction. Although AATD accounts for approximately 1% of chronic obstructive pulmonary disease (COPD) cases and up to 2% of emphysema, AATD-related COPD remains largely underdiagnosed, despite guideline recommendations for systematic evaluation in patients with COPD, particularly in high-risk clinical settings. Pathologically, AATD-related COPD is not limited to the typical early-onset, lower-lobe-predominant emphysema, also including upper-lobe or mixed emphysema patterns, airway-predominant disease, small airways dysfunction, and bronchiectasis. Clinically, AATD-related COPD is distinguished from smoking-related COPD by its earlier onset, physiological impairment that is often disproportionate to smoking exposure, and its potential presence of certain extrapulmonary manifestations. Diagnosis and monitoring are also challenged by the frequent discordance between airflow limitation and gas transfer impairment, as well as the early involvement of small airways, limiting reliance on spirometry alone. A multimodal assessment incorporating more sensitive functional techniques and CT densitometry may provide a more precise evaluation of disease burden, progression, and prognosis. Management generally follows standard COPD principles, with intravenous AAT augmentation therapy remaining currently the only established disease-modifying therapy for selected patients with severe deficiency. The advent of new pharmacological and gene-based therapies emphasizes the importance of developing personalized management strategies that integrate genotype and longitudinal disease behavior. This narrative review summarizes current evidence on AATD-associated COPD, focusing on its genetic basis and pathophysiological features, clinical and functional heterogeneity, current and emerging diagnostic and monitoring approaches, and disease-specific management considerations.

Background/Objectives: The coexistence of chronic obstructive pulmonary disease (COPD) and type 2 diabetes mellitus (T2D) poses significant clinical challenges due to overlapping mechanisms of systemic inflammation, oxidative stress, hypoxia, and metabolic dysregulation. Patients with both conditions face higher risks of exacerbations, prolonged hospitalizations, cardiovascular events, and reduced quality of life. This review aims to summarize current evidence on the pathophysiological interplay between COPD and T2D and to evaluate the impact of lifestyle and pharmacologic interventions. Methods: A narrative review of the literature was conducted to evaluate the pathophysiological links between COPD and T2D, assess the effects of pharmacologic and lifestyle interventions, and highlight key gaps and priorities for future research, with an emphasis on integrated, evidence-based management for this high-risk population. Results: Lifestyle interventions, including smoking cessation and structured physical activity, remain foundational to management. Emerging evidence indicates that antidiabetic therapies, such as glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT-2is), may confer additional pulmonary, metabolic, and cardiovascular benefits. These agents modulate systemic inflammation, oxidative stress, endothelial function, and insulin sensitivity, potentially reducing COPD exacerbations, improving lung function, and enhancing survival. Safety concerns, including glucocorticoid-induced hyperglycaemia and hypoxia-related metabolic complications, underscore the need for careful monitoring and individualized therapy COPD patients. Conclusions: Optimal care requires a multidisciplinary, patient-centred approach integrating pulmonology, endocrinology, primary care, nutrition, and rehabilitation, alongside shared decision-making and patient education. Despite promising findings, critical knowledge gaps remain. Large, well-designed randomized controlled trials and standardized definitions are needed to guide personalized therapeutic strategies.

BACKGROUND:Lifestyle choices may affect the pathogenesis and/or clinical expression of asthma. Certain dietary habits such as the Mediterranean diet (MD), possibly through pro-inflammatory effects may be implicated. OBJECTIVE:To assess the association between adherence to MD and asthma control in severe asthmatics. METHODS:During the period between March 2022 and 2023, patients with severe asthma from 16 pulmonary centers all over Greece were recruited. Adherence to MD was assessed through a short interviewer-administered questionnaire, the MD Adherence Screener, previously validated in Mediterranean populations. The level of asthma control was assessed by the Asthma Control Test. A multiple logistic regression model was applied, adjusting for gender, age, body mass index, corticosteroid intake, comorbidities, and treatment. RESULTS:The study sample included 315 severe asthmatics (30% males) with mean age 56.6 years (standard deviation, S.D. = 14.3 years). There is an indication, albeit not statistically significant, that higher adherence to MD was associated with better asthma control in patients with severe asthma (OR: 1.19, 95% CIs: 0.61, 2.34). Furthermore, controlling for the patients' personal characteristics and dietary habits, other diet related conditions and metabolic diseases, such as obesity or diabetes, were significantly associated with poorer asthma control. CONCLUSIONS:In a cross-sectional study undertaken in a Mediterranean population, we observed a positive, but not statistically significant, association between higher adherence to MD and better asthma control in severe asthmatic patients. However, our findings are limited by the study design which does not allow us to infer causality and by the use of a screener to assess adherence to MD.

Background Severe asthma (SA) imposes a disproportionate burden on patients and healthcare systems worldwide, yet region-specific data from Southern Europe remain scarce. The Greek Severe Asthma Registry (GSAR), an initiative of the Hellenic Thoracic Society, provides the first nationwide characterisation of severe asthma in Greece. Methods We analysed data cross-sectionally from 619 adult patients (median age: 56 years; 61.1% female) with severe asthma, recruited across 13 specialised hospital centres and 11 private respiratory practices between March 2018 and November 2021. Patients were stratified by age of asthma onset, biologic therapy use and maintenance oral corticosteroid (mOCS) dependence. Clinical, inflammatory and treatment characteristics were assessed, alongside exacerbation predictors. Results The study population exhibited substantial disease burden, with 434 patients (70.1%) experiencing ≥1 exacerbation and 149 (24.1%) requiring hospitalisation in the prior year. Late-onset asthma (60.7%) was associated with a faster progression to severe disease, higher exacerbation risk (79.8% versus 69.5%, p=0.004), and more frequent cardiometabolic comorbidities versus early-onset asthma. Despite better asthma control (Asthma Control Test ≥20: 61.8% versus 50.5%, p=0.012), biologically treated patients (57%) had more severe disease, including lower forced expiratory volume in 1 s (FEV 1 ) % predicted (73% versus 81%, p<0.001). Patients receiving mOCS (18.9%) exhibited poorer asthma control, higher exacerbation rates and more frequent corticosteroid-related comorbidities. In multivariable models, elevated blood eosinophil count (incidence rate ratio: 1.044 per 100 cells per μL) and reduced FEV 1 % (odds ratio: 0.97 per 1% increase) were independent predictors of exacerbations. Conclusions This study highlights the phenotypic heterogeneity of severe asthma in Greece and reveals region-specific treatment patterns and unmet clinical needs despite access to advanced therapies. These real-world findings may guide national asthma care strategies and contribute to European initiatives aimed at optimising asthma management.

Purpose:Time to biologic initiation for the treatment of severe asthma (SA) is affected by many factors, including ease of access to biologics, which is often subject to approval by regulatory authorities and reimbursement criteria by relevant agencies. We investigated the association between ease of biologic access (using the biologic accessibility score [BACS] as a proxy) and post-biologic asthma outcomes, including remission. Methods:This ecological study, using data from CHRONICLE (a US severe asthma registry), the International Severe Asthma Registry (ISAR), and the Optimum Patient Care Research Database (OPCRD), included patients with SA from 21 countries. Associations at the country level, between BACS, a composite score of prescription criteria for biologics in SA, and the proportion of patients with a favorable asthma outcome 1-year post-biologic in each setting (ie ISAR country or in the CHRONICLE or OPCRD datasets) were tested. Several definitions of favorable outcome were used, including proportion of patients who achieved clinical remission (defined using 2, 3 and 4 domains), experienced no exacerbations, had well- or partly controlled asthma, a percent predicted forced expiratory volume in 1 second (ppFEV1) or percent predicted peak expiratory flow rate (ppPEFR) ≥80%, and no long-term oral corticosteroid (LTOCS) use. Results:A total of 9,183 patients were included. A higher BACS (as a proxy of easier access to biologics) was associated with a higher likelihood of achieving clinical remission (p≤0.001), no exacerbations (p<0.001), well- or partly controlled asthma (p=0.047), a ppFEV1 or ppPEFR ≥80% (p=0.004), and no need for LTOCS (p=0.045) 1 year post-biologic initiation. Conclusion:Easier access to biologics for patients with SA, a prerequisite for shorter time-to-initiation, was associated with a greater probability of achieving clinical remission and other favorable asthma outcomes. Initiating biologics earlier in the asthma disease course may help unlock greater therapeutic potential in SA. These findings warrant confirmation in additional studies to further establish the causal relationship between biologic accessibility, timing of initiation, and clinical outcomes in SA.

Epigenetic mechanisms refer to heritable and potentially reversible modifications that regulate chromatin architecture and gene expression without altering the underlying DNA sequence. In asthma, these mechanisms provide a molecular interface between genetic susceptibility, environmental exposures, and immune dysregulation, contributing to disease heterogeneity and treatment response. The treatable traits paradigm, which focuses on the identification of specific modifiable biological and clinical characteristics, offers a clinically relevant framework for linking epigenetic changes to distinct molecular endotypes, enhancing mechanistic stratification beyond traditional phenotyping, thereby supporting precision medicine approaches. Emerging evidence suggests that epigenetic signatures have considerable potential as biomarkers for inflammatory endotyping and therapeutic stratification, although further validation is required before routine clinical implementation. In this mini review we will discuss epigenetic mechanisms involved in the development and maintenance of asthma processes, such as DNA methylation, histone modifications, and noncoding RNAs, focusing on their relevance to key treatable traits, including type 2 inflammation, corticosteroid responsiveness, airway remodeling, and exposure-driven disease.

IntroductionDespite their profound clinical impact and high mortality, acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF) still lack any effective or standardized treatment strategies. This manuscript describes the rationale and design of a randomized, multicenter, open-label Phase III clinical trial evaluating the efficacy of intravenous immunoglobulin (IVIG) compared with usual care in hospitalized patients with AE-IPF.MethodsThis trial will enroll 196 patients across eight different sites in Greece. Inclusion criteria are designed to identify patients with AE-IPF according to the American Thoracic Society definition, while excluding those with cardiac decompensation or pulmonary embolism. The primary endpoint is a composite of all-cause in-hospital mortality or the need for intubation. Secondary endpoints include all-cause mortality at 30 and 90 days, hospital readmission or a new AE-IPF episode within 90 days, and the change in the PaO2/FiO2 ratio from hospital admission to discharge.DiscussionBased on the concept that patients with IPF frequently demonstrate impaired cellular and humoral immunity, and inflammation and/or immune dysregulation may contribute to AE-IPF pathogenesis, there is a strong rationale for evaluating the therapeutic usefulness of IVIG in this setting. Retrospective data indicate that IVIG could provide clinical benefit in AE-IPF, potentially through its anti-inflammatory and immunomodulatory effects. In this trial, IVIG will be administered as an adjunct to usual care, which includes pulse corticosteroids, broad-spectrum antibiotics, prophylactic anticoagulation, and oxygen therapy. This intervention has the potential to significantly influence current treatment strategies for AE-IPF.Clinical trial registrationhttps://clinicaltrials.gov/, identifier NCT07299695.

OBJECTIVE:The objective of this study is to describe and compare the clinical characteristics, treatment approaches, and associated comorbidities of patients with severe asthma across Greece, Southern Europe, and the global population. This comparative approach aims to enhance the understanding of region-specific differences and similarities among patients living with severe asthma. METHODS:Data from the International Severe Asthma Registry (ISAR) were analyzed across three cohorts: Greek, Southern European, and Global. Variables included demographics, baseline characteristics, age at asthma onset, medication use, lung function, exacerbation history, biomarkers, and comorbidities. RESULTS:A total of 16,063 patients from the global ISAR dataset, 3406 from Southern Europe, and 206 from Greece were included. Greek patients had a lower mean annual exacerbation rate (1.24 ± 1.67) compared with the global cohort (1.84 ± 2.58, p = 0.001) and Southern Europe (1.73 ± 2.56, p = 0.052). Uncontrolled asthma was most prevalent in Greece (60.32%) versus Southern Europe (35.58%, p < 0.001) and the global cohort (57.07%, p = 0.034). Long-term oral corticosteroid use was less frequent in Greece (24.73%) and in global cohort (21.50%, p = 0.287) than in Southern Europe (52.04%, p < 0.001). The prevalence of eosinophilic phenotype was high in all cohorts. However, in Greece, it was lower compared to Southern Europe (73.55% vs. 89.89% p < 0.001) and globally (73.55% vs. 83.34%, p = 0.011). Greek patients also demonstrated lower fractional exhaled nitric oxide (FeNO) levels and lower eosinophil counts than Southern Europe, along with reduced biologic therapy initiation (56.31%) compared to Southern Europe (74.02%, p < 0.001) but higher than global rates (48.40%, p = 0.024). CONCLUSIONS:Regional differences in severe asthma underline the importance of tailored treatment approaches, and multidisciplinary management of comorbid conditions.

The association between severe asthma and obesity is well established, as higher body mass index (BMI) is associated with higher prevalence and incidence of severe asthma. Biologic agents have been recently developed for severe asthma treatment. However, the efficacy of biologic agents in patients with higher BMI is not well studied. The aim of this systematic review was to determine whether there is an association between BMI and the response to five novel biologic agents. Our study design followed the PRISMA guidelines. A literature search was performed using the PubMed/Medline and the Scopus databases up to May 2025 for the following agents: mepolizumab, benralizumab, dupilumab, reslizumab, and tezepelumab. After meticulous screening, 21 articles were selected. Studies on mepolizumab showed that higher BMI was associated with failure to achieve clinical remission, while BMI < 30 kg/m2 was associated with better clinical outcomes. Regarding benralizumab, significant improvements were observed in respiratory symptoms and reductions in annual asthma exacerbation rate for patients with BMI ≤ 35 kg/m2 but not for patients with BMI > 35 kg/m2. One study about dupilumab describes it as equally effective across all BMI levels. Reslizumab appears to be effective across different BMI levels; however, effectiveness seems to decrease in patients with high BMI. Regarding tezepelumab, no study was found. Biologic agents are effective treatments for severe asthma, although mepolizumab, benralizumab, and reslizumab appear to have better results in patients with lower BMI. Dupilumab appears to be equally effective across all BMI categories, while no data are available for tezepelumab. More studies in patient populations with severe asthma and comorbid obesity are needed to evaluate the effectiveness of biologic therapies in this specific category of patients. Registration and protocol: PROSPERO CRD42024609708. Individuals with obesity are more likely to have severe asthma, as higher body weight is often linked to worse asthma symptoms. Biologic agents have recently been developed to target specific inflammatory pathways that are activated in patients with severe asthma. However, it remains unclear whether these medications are equally effective in patients with and without obesity. In this study, we aimed to examine the association between body mass index (BMI) and the response to five of the most commonly prescribed biologic agents (mepolizumab, benralizumab, dupilumab, reslizumab, and tezepelumab). Our findings suggest that BMI may influence the effectiveness of some biologic agents, as mepolizumab, benralizumab, and reslizumab appear to work better in patients with lower BMI. Yet, dupilumab appears to be equally effective in all patients, regardless of their BMI. No studies on tezepelumab in patients with asthma and comorbid obesity met our inclusion criteria. Future research is needed to identify the most effective medications across different BMI categories.

Cellular senescence is a stress-induced type of irreversible cell cycle arrest, driven by telomere attrition, oxidative stress, DNA damage, mitochondrial dysfunction, oncogene activation, and chronic inflammation. Senescent cells remain metabolically active, secreting cytokines, chemokines, growth factors, matrix metalloproteinases, extracellular vesicles and oxidative mediators, comprising a senescence-associated secretory phenotype (SASP) that affects the tissue microenvironment. With aging, impaired immune clearance results in senescent cell accumulation, promoting inflammation, immunosuppression and fibrosis. Emerging evidence implicates cellular senescence in obstructive airway diseases, reflecting the lung’s continuous exposure to environmental and oxidative insults, and several pathways, including DNA damage response and p53/p21 and p16INK4a signaling, telomere dysfunction, reactive oxygen species production, and mitochondrial defects, integrate stress signals to enforce senescence. In chronic obstructive pulmonary disease, a SASP-associated inflammatory milieu supports stress-induced tissue injury, while uncertainty still exists about the effects of chronic SASP on tumor suppression versus tumor promotion. In asthma, senescence processes have been associated with both Type(T)2-high and T2-low endotypes, underlying the interplay between environmental exposures, airway epithelial dysfunction and induced senescence mechanisms. Finally, in bronchiectasis, the neutrophilic, dysbiotic airway environment links dysregulated senescence with disease persistence and progression. Conventional therapies, antioxidants, serine protease inhibitors and novel senotherapeutic strategies represent promising approaches for therapeutic interventions.

Background: Remission of asthma can occur as part of the natural history of the disease; however, the use of biologics can result in disease remission in some patients. Objective: In this post hoc analysis of the RELIght study, we aimed to evaluate clinical remission in real life among patients treated with mepolizumab, to detect possible differences between "remitters" and "nonremitters," and to evaluate possible predictors of remission. Methods: Clinical remission was defined as the absence of asthma exacerbations, discontinuation of oral corticosteroids (OCS), achievement of asthma control (Asthma Control Test [ACT] ≥ 20), and stable or improved lung function. Results: A total of 146 patients were evaluated; remission was achieved in 40 (27.4%) and 29 (22%) after 12 and 24 months, respectively. At 12 months, the patients in remission had a better baseline ACT score (17.0 [14.0-19.0] versus 15.0 [12.0-17.0]; p = 0.027), were more rarely using OCS (35% versus 62.2%; p = 0.004), and required a lower baseline dose of OCS (5.0 mg/day [5.0-10.0 mg/day] versus 10.0 mg/day [5.0-15.0 mg/day]; p = 0.042) at baseline, whereas, at 24 months, they less frequently carried a baseline diagnosis of gastroesophageal reflux disease (GERD) (10.3% versus 32%; p = 0.031) and used lower doses of OCS at baseline (5.0 [1.0-5.0] versus 10.0 [5.0-15.0]; p = ≤0.001) versus nonremitters; 52.5% of patients had sustained remission, whereas 42.5% experienced relapse. These patients more frequently had GERD versus patients with sustained remission (52.9% versus 4.8%; p = 0.002). Finally, regression analysis has shown that GERD was the only predictor of relapse. Conclusion: Remitters had better asthma control and needed lower doses or no maintenance OCS at baseline, whereas GERD seems to be an important factor that affects remission and relapse.Clinical trial NCT04084613, www.clinical trials.gov.

Exacerbations of Chronic Obstructive Pulmonary Disease (COPD) have a substantial effect on overall disease management, health system costs, and patient outcomes. However, exacerbations are often underdiagnosed or recognized with great delay due to several factors such as patients’ inability to differentiate between acute episodes and symptom fluctuations, delays in seeking medical assistance, and disparities in dyspnea perception. Self-management intervention plans, telehealth and smartphone-based programs provide educational material, counseling, virtual hospitals and telerehabilitation, and help COPD patients to identify exacerbations early. Moreover, biomarkers such as blood eosinophil count, fibrinogen, CRP, Serum amyloid A(SAA),together with imaging parameters such as the pulmonary artery-to-aorta diameter ratio, have emerged as potential predictors of exacerbations, yet their clinical utility is limited by variability and lack of specificity. In this review, we provide information regarding the importance of the early identification of exacerbation events in COPD patients and the available methods which can be used for this purpose.

BACKGROUND:Severe asthma with an eosinophilic phenotype (SAEP) and chronic rhinosinusitis with nasal polyps (CRSwNP) are predominantly type 2-driven diseases, characterised by eosinophilic inflammation and substantial disease burden. Mepolizumab, a humanised monoclonal antibody that targets interleukin-5, a key cytokine in type 2 inflammation, is an effective, approved treatment both in SAEP and CRSwNP. We aimed to analyse real-world evidence of mepolizumab effectiveness in patients with comorbid SAEP and CRSwNP. METHODS:This study pooled five existing, predominantly European cohorts to describe the impact of mepolizumab on the rate of clinically significant exacerbations (CSEs) and other outcomes in adults with SAEP without and with comorbid CRSwNP (SAEP[-]CRSwNP and SAEP[+]CRSwNP, respectively). RESULTS:Overall, 1037 patients were included. Baseline characteristics were similar in both cohorts. Mepolizumab was associated with a reduction from baseline in the annual rate of CSEs at 12-months post-initiation (SAEP[-]CRSwNP: 72.7%; SAEP[+]CRSwNP: 79.7%), irrespective of baseline blood eosinophil count (BEC). When patients with SAEP[+]CRSwNP were compared with patients with SAEP[-]CRSwNP, a 30.0% incremental benefit in the reduction of CSEs was observed. At 12-months post-initiation, mepolizumab was also associated with a reduction in oral corticosteroid use and BEC, and an improvement in lung function and Asthma Control Test (ACT) scores in both cohorts. Post-mepolizumab initiation, ≥ 3 clinical remission criteria were fulfilled by 47.2% and 52.3% of patients with SAEP[-]CRSwNP and SAEP[+]CRSwNP, respectively. CONCLUSIONS:The results provide a greater understanding of mepolizumab's effectiveness, demonstrating a substantial improvement in asthma outcomes, irrespective of baseline BEC and the presence of comorbid CRSwNP.

Background: Asthma characterization using blood eosinophil count (BEC) (among other biomarkers and clinical indices) is recommended in severe asthma (SA), but the masking effect of oral corticosteroids (OCS), makes this challenging. Aim: Our aim was to explore the effect of OCS use (both intermittent [iOCS] and long-term [LTOCS]) prior to biologic initiation on SA phenotype and biomarker profile in real-life and to characterize the burden of SA among patients prescribed LTOCS by biomarker profile. Methods: This was a registry-based cohort study, including data from 23 countries collected between 2003 and 2023 and shared with the Internatonal Severe Asthma Registry (ISAR). Patients with SA were categorized into 3 cohorts, those with: (i) no prescription for OCS, (ii) prescription(s) for iOCS (ie, ≤90 days in previous 12-months, usually short courses for exacerbations), and (iii) prescriptions for LTOCS (ie, >90 days in previous 12-months). Biomarker distribution (ie, BEC, fractional exhaled nitric oxide [FeNO], and total Immunoglobulin E [IgE]) were quantified in the year prior to biologic initiation in patients with SA according to OCS prescription pattern. Phenotypes were characterized for those prescribed LTOCS according to BEC cut-off (<150 and ≥ 150 cells/μL). Results: Of 4305 patients included, 5.0% (n = 215), 54.1% (n = 2330) and 40.9% (n = 1760) were prescribed no OCS, iOCS, and LTOCS, respectively. The BEC distribution varied by prescription pattern and LTOCS dose (<5 mg to ≥20 mg/day); BEC was <150 cells/μL in 28.6% (n = 369/1288) of LTOCS patients, compared to 19.5% (n = 284/1460) of iOCS patients and 14.0% (n = 21/150) of those in the no OCS group. Median BEC was also significantly lower in the LTOCS versus the iOCS group (310 vs 400 cells/μL; p < 0.001). A similar pattern was noted for IgE, but not FeNO. Among LTOCS patients with BEC <150 cells/μL, 39.9% experienced ≥4 exacerbations, 75.1% had uncontrolled asthma symptoms and 55.9% had evidence of persistent airflow obstruction (compared with 40.9%, 76.2% and 59.5% of those with BEC ≥150 cells/μL, respectively). Conclusions: OCS, whether prescribed intermittently or long term, affect BEC distribution potentially leading to heightened risk of phenotype misclassification and influencing subsequent treatment decisions. FeNO appears to be less susceptible to OCS-induced suppression. Disease burden was high for those in the LTOCS group and was high independent of dose and BEC. Our findings highlight the importance of considering OCS use, even intermittent use, when characterizing SA, and suggests the need for earlier phenotyping and alternative treatment strategies for LTOCS patients with low BEC.

Severe asthma imposes a significant burden on public health worldwide, mainly due to its morbidity and high cost. The management of severe asthma has dramatically changed in the past few years with the introduction of biologics. Zero exacerbations, zero systemic corticosteroids, better asthma control, and better lung function are the outcomes that the era of biologics has made attainable in a large proportion of severe asthmatics, ending up in a better quality of life. Still, even today, the changes at the tissue level that reflect these outcomes are not that clear. As a chronic inflammatory disease, asthma often involves airway remodeling in its severe forms; endobronchial biopsies may provide critical insights into these tissue-level changes before and after biologic treatment. However, bronchoscopy is an invasive tool for severe asthma, thus limiting its use in daily clinical practice. This review focuses on summarizing the changes that biologics exert in biopsies obtained from severe asthmatics under biological treatment, providing an opportunity to shed light on what really happens there where it is not easy to see, and especially on what does not happen in patients under biologics who fail to respond as expected. Moreover, the armamentarium of biomarkers used for making the proper choice in patients eligible for more than one biologic needs to be enriched. Biopsy-related markers could be an ideal adjunct to the current ones—blood eosinophils, FeNO, and IgE—to assist the clinician to choose the right biologic for the right patient with severe asthma to achieve disease remission.

During the coronavirus disease-19 (COVID-19) pandemic, there was an unprecedented requirement for hospital bed availability. The present study aimed to examine the characteristics and outcomes of patients hospitalized in a COVID-19 unit that operated as a novel middle-step unit in Greece. The present study aimed to determine whether the middle-step unit supported the central general hospitals; thus, highlighting the potential of these models in future pandemics. During the 9-month period of operation, a total of 631 patients were admitted. In addition, 539 (85.4%) patients were discharged, 57 (9%) patients were referred to surrounding hospitals for further management and 35 (5.6%) patients succumbed. Based on the results of the present study, an algorithm for patient referral to middle-step units was outlined for future pandemics.

Chronic obstructive pulmonary disease (COPD) is a common and complex disease characterized by persistent airflow limitation and the presence of exacerbations, resulting in significant morbidity and mortality. Although the pathogenesis of COPD is multifactorial, airway inflammation plays a significant role in disease progression. Despite the advantages of non-pharmaceutical and pharmaceutical interventions that have significantly improved the symptom burden and exacerbation frequency in COPD, there is a lack of disease-modifying therapies that target the underlying disease mechanisms. Monoclonal antibodies (mAbs), a drug class that has improved treatment in severe asthma by blocking mediators of the type 2 (Th2) and allergic inflammatory cascades, are currently under investigation for their efficacy in COPD. Our review summarizes the evidence for the use of monoclonal antibodies in COPD and discusses current limitations and promising advances. Although targeting Th1 inflammation has failed to improve COPD outcomes, recent clinical trials have shown beneficial effects of monoclonal antibodies targeting Th2 inflammation, providing evidence for a personalized approach in COPD treatment.

Chronic obstructive pulmonary disease (COPD) is characterized by the presence of comorbidities, such as cardiovascular diseases, that significantly impact symptoms, quality of life and prognosis. Indeed, it is shown that patients with COPD may present with diseases of aging, earlier in life, including eye disorders, such as macular degeneration and cataract. Although underrecognized, cumulative evidence over the last years suggests that COPD is associated with ocular abnormalities, mainly in the posterior segment of the eye, affecting both the microvascular network of the retina and the optic nerve, while structural abnormalities of the choroid and cornea have also been described. Thus, the aim of this review is to provide a comprehensive description of the evidence for ocular findings in patients with COPD that is an underrecognized entity and co-morbidity. A secondary aim of this review is to introduce pulmonologists to current ophthalmological techniques that may foster both clinical practice and research, especially through the assessment of the ocular microvascular network that is closely related to cardiovascular comorbidities.